ライフサイエンスコーパス: NMJ

1 NMJ decline occurs in aged animals and may appear before

2 NMJ deficits are aggravated in these mice when compared

3 NMJ formation requires intimate communications among the

4 NMJ formation requires intimate interactions among moton

5 NMJ-in-a-dish models have been developed to examine huma

6 proved muscle re-innervation (27.9% vs 38.0% NMJs re-innervated; p < 0.02); reduced muscle atrophy (1

7 ry compared with controls (N = 30; n = 1,165 NMJs).

8 FGFBP1 from SOD1(G93A) mice also accelerates NMJ degeneration and death.

9 Model animals had fewer active NMJs, detectable by endplate recordings, compared with a

10 MP matrices produce more functionally active NMJs-in-a-dish, which could be used to elucidate disease

11 In addition, NMJs of adult transgenic mice that expressed excess axon

12 hanisms governing tSC occupancy of the adult NMJ and for conditions that adversely affect tSCs.

13 a Piccolo-Bassoon-Piccolo structure in adult NMJs.

14 lly ablated SCs during development and after NMJ formation to investigate the consequences of the abl

15 Finally, ablation of SCs at P30, after NMJ maturation, led to NMJ fragmentation and neuromuscul

16 By contrast, amphibian NMJs do not show such degeneration even though they can

17 acetylcholine receptor (AChR) clustering and NMJ (neuromuscular junction) formation.

18 s an E3 ligase to induce AChR clustering and NMJ formation, possibly by regulation of AChR neddylatio

19 cesses between NMJs to guide axon growth and NMJ reinnervation.

20 dUGP mutants display striking locomotor and NMJ formation defects, including expanded synaptic arbou

21 minal Schwann cell (tSC) injury response and NMJ recovery with inhibition of: (1) macrophage recruitm

22 ults in loss of specific axonal branches and NMJs formed by one motor neuron, MNISN-1s, while other b

23 ort that HDAC6 preferentially accumulates at NMJs and that it contributes to the organization and the

24 ted, rapsyn fails to associate with AChRs at NMJs of living mice.

25 e experiments define synaptic dysfunction at NMJs experiencing ALS-related degradation and demonstrat

26 we demonstrate critical roles for FGFBP1 at NMJs in developing, aging and SOD1(G93A) mice.

27 growth factor binding protein 1 (FGFBP1) at NMJs.

28 growth factor binding protein 1 (FGFBP1) at NMJs.

29 , alters the rate of loss of motor inputs at NMJs during developmental synapse elimination.

30 aptic arborization and active zone number at NMJs following C9orf72 transgenic expression in motor ne

31 ar disease, such as spinal muscular atrophy, NMJ disorder and muscular dystrophy.

32 d expression of rapsyn in muscles attenuated NMJ deficits of HSA-Lmna-/- mice.

33 and expressing rapsyn in muscles attenuated NMJ deficits of HSA-Lmna-/- mice.

34 Because NMJ denervation occurs early in the process and that per

35 in skeletal muscles during aging and before NMJ degeneration in SOD1(G93A) mice, a mouse model for a

36 WT mice, before signs of MN death and before NMJ morphological alterations.

37 development, its expression decreases before NMJ degeneration during aging and in SOD1(G93A) mice, a

38 Yet, direct links between NMJ pathways and ALS-associated genes such as FUS, whose

39 y, tSCs extend cytoplasmic processes between NMJs to guide axon growth and NMJ reinnervation.

40 modeling, suggesting a mechanism utilized by NMJs in dry season toads to support quick recover from t

41 ophy (P < 0.0001) in patients with cachexia, NMJ morphology was fully conserved.

42 f the C. elegans SMN ortholog, SMN-1, causes NMJ defects.

43 the present study, we examined and compared NMJ morphology of toads obtained from the wild during th

44 ting soft and stiff stripes improves current NMJ-in-a-dish models by inducing both mouse and human my

45 cytoplasmic process extension and decreased NMJ reinnervation compared with saline controls.

46 rmation will shed light on whether defective NMJs might contribute to the loss of motor function and

47 ity because they were inserted at denervated NMJs.

48 ended disorganized processes from denervated NMJs and failed to initiate or guide nerve terminal spro

49 o adopt a phagocytic phenotype on denervated NMJs in SOD1(G37R) mice.

50 tic profile (MUSP) that reports MU-dependent NMJ synaptic properties.

51 Finally, differences in these PSC-dependent NMJ repair mechanisms were MU type dependent, thus refle

52 treatment increased the number of detectable NMJs during endplate recording.

53 yb2 (with Syb2 being dominant) in developing NMJs in mice.

54 amate have been shown to regulate Drosophila NMJ physiology by modulating the clustering of postsynap

55 cally and postsynaptically at the Drosophila NMJ and that it is a presynaptic regulator of rapid acti

56 cterized C9orf72 pathology at the Drosophila NMJ and utilized several approaches to restore synaptic

57 until a single motor neuron innervates each NMJ.

58 ion of pre and postsynaptic elements in each NMJs from both the dry and wet season were compared.

59 factor-A (Vegf-A) is crucial to establishing NMJ reinnervation at the end target muscle.

60 S, FR, and FF NMJs of WT mice showed distinct synaptic properties from

61 In the absence of FGFBP1, NMJs exhibit structural abnormalities in developing and

62 ss in a manner that would be detrimental for NMJ repair.

63 utions of the immune system are integral for NMJ reinnervation and functional muscle recovery after n

64 indicate that SCs are not only required for NMJ formation, but also necessary for its maintenance; a

65 rp4, two cell surface receptors required for NMJ formation.

66 r transmission at the most highly fragmented NMJs in the diaphragms of old (26-28 months) mice is, if

67 te that the presynaptic terminal of the frog NMJ has a very brief AP waveform and that the motor nerv

68 Although the frog NMJ is a model synapse for the study of synaptic transmi

69 tter release previously reported at the frog NMJ.SIGNIFICANCE STATEMENT The AP waveform plays an esse

70 presynaptic terminal of male and female frog NMJs and shown that the AP is very brief in duration and

71 lmarks of disease, including motor function, NMJ pathology and motor neuron cell preservation.

72 tor neurons self-organize to form functional NMJ connections.

73 results propose a mechanism whereby further NMJ and skeletal muscle decline ensues upon SC depletion

74 ple method to model and evaluate adult human NMJ de novo development or disease in culture.

75 At the human NMJ, a delay in synaptic maturation and an altered maint

76 These results reveal a role of lamin A/C in NMJ maintenance and suggest that nuclear dysfunction or

77 These results reveal a role of lamin A/C in NMJ maintenance and suggest that nuclear dysfunction or

78 However, changes in NMJ properties as a function of MU types remain debated.

79 Defects in NMJ formation during development or maintenance in adult

80 Deficits in NMJ formation and maintenance cause neuromuscular disord

81 We review recent findings in NMJ formation, maintenance, neuromuscular disorders, and

82 hysiological role of Wnt-MuSK interaction in NMJ formation and function remains to be elucidated.

83 an active contribution of skeletal muscle in NMJ dysfunction.

84 he implications of the converged pathways in NMJ formation and liver cancer.

85 n (NMJ) in mice, but their specific roles in NMJ formation and function remain unclear.

86 ized, less is known about the role of SCs in NMJ formation and maintenance.

87 This study reveals a critical role of SCs in NMJ formation as well as maintenance.

88 The role of Schwann cells (SCs) in NMJ formation and maintenance was not well understood.

89 oteins essential for active zone assembly in NMJs, ribbon synapses, and brain synapses.

90 In contrast, the Piccolo levels in NMJs from aged mice were comparable to levels in adult m

91 eration mechanism of active zone proteins in NMJs from aged mice.

92 on protein levels decreased significantly in NMJs from aged mouse.

93 salbutamol can prolong survival and increase NMJ number in a severe model of DOK7-CMS.

94 The underlying hypothesis, that increasing NMJ fragmentation is associated with impaired transmissi

95 ing the structure and function of individual NMJs, we show that neuromuscular transmission at the mos

96 pal LTP deficits and neuromuscular junction (NMJ) abnormalities, characterized by decreased size and

97 n motor neurons, the neuromuscular junction (NMJ) and muscle fibres.

98 he Drosophila larval neuromuscular junction (NMJ) as a model, we provide evidence that NPRRs recapitu

99 ) at the adult mouse neuromuscular junction (NMJ) by using mice expressing diphtheria toxin receptor

100 eficits, progressive neuromuscular junction (NMJ) denervation and pre-synaptic build-up of mutant Gly

101 ns (MNs) preceded by neuromuscular junction (NMJ) denervation.

102 e reversal of normal neuromuscular junction (NMJ) development where AChR clustering precedes innervat

103 study of adult human neuromuscular junction (NMJ) development, a process requiring maturation of musc

104 oordinated movement, neuromuscular junction (NMJ) development, synaptic glycosylation, and Wnt trans-

105 Neuromuscular junction (NMJ) disruption is an early pathogenic event in amyotrop

106 protein, leading to neuromuscular junction (NMJ) dysfunction and spinal motor neuron (MN) loss.

107 eptor in muscles for neuromuscular junction (NMJ) formation.

108 Although the frog neuromuscular junction (NMJ) has long been a model synapse for the study of neur

109 ed at the developing neuromuscular junction (NMJ) in mice, but their specific roles in NMJ formation

110 cells (SCs), at the neuromuscular junction (NMJ) in mice.

111 ynaptic sites at the neuromuscular junction (NMJ) in vivo remains largely unknown.

112 me without affecting neuromuscular junction (NMJ) integrity.

113 ctivity; because the neuromuscular junction (NMJ) is a cholinergic synapse, acetylcholine has been as

114 melanogaster larval neuromuscular junction (NMJ) is a model synapse with robust expression of homeos

115 The neuromuscular junction (NMJ) is a specialized synapse that is the point of conne

116 The neuromuscular junction (NMJ) is a synapse formed between motoneurons and skeleta

117 The neuromuscular junction (NMJ) is a tripartite synapse that is formed by motor ner

118 transmission at the neuromuscular junction (NMJ) is an aspect of CMT2D.

119 CANCE STATEMENT: The neuromuscular junction (NMJ) is critical for all voluntary movement.

120 ICANCE STATEMENT The neuromuscular junction (NMJ) is designed to faithfully elicit a muscular contrac

121 The neuromuscular junction (NMJ) is one of the best-studied cholinergic synapses.

122 A hallmark of the neuromuscular junction (NMJ) is the high density of acetylcholine receptors (ACh

123 The neuromuscular junction (NMJ) is the site of a number of autoimmune and genetic d

124 he morphology of the neuromuscular junction (NMJ) is typically affected by neuromuscular disease, whe

125 cal targeting of the neuromuscular junction (NMJ) may play a key role in cachexia, but this has yet t

126 roles of Mmp at the neuromuscular junction (NMJ) model synapse in the reductionist Drosophila system

127 Denervation of the neuromuscular junction (NMJ) precedes the loss of motor neurons (MNs) in amyotro

128 The neuromuscular junction (NMJ) provides the interface between nerve and muscle and

129 ediated response for neuromuscular junction (NMJ) reinnervation following nerve injury and repair.

130 larval glutamatergic neuromuscular junction (NMJ) represents a powerful synaptic model to investigate

131 At the glutamatergic neuromuscular junction (NMJ) synapse, we find that Notum secreted from the posts

132 interacting via the neuromuscular junction (NMJ) within a microfluidic device.

133 can also impact the neuromuscular junction (NMJ), a synapse that transmits signals from motoneurons

134 he Drosophila larval neuromuscular junction (NMJ), at which glutamate acts as the excitatory neurotra

135 At the neuromuscular junction (NMJ), early alterations in perisynaptic Schwann cell (PS

136 sicle cycling in the neuromuscular junction (NMJ), end-plate structure of NMJs and muscle contractili

137 ally modified at the neuromuscular junction (NMJ), hence increasing their stability.

138 synaptic glia of the neuromuscular junction (NMJ), that participate in synapse development, function,

139 at in the Drosophila neuromuscular junction (NMJ), the endocytic scaffolding protein Dap160 colocaliz

140 y takes place at the neuromuscular junction (NMJ), the output of motor neurons, but its impact on NMJ

141 the formation of the neuromuscular junction (NMJ), while y-z- agrin is widely expressed and has diver

142 ay at the Drosophila neuromuscular junction (NMJ).

143 tudied at the rodent neuromuscular junction (NMJ).

144 ive weakening of the neuromuscular junction (NMJ).

145 usion at presynaptic neuromuscular junction (NMJ).

146 and function at the neuromuscular junction (NMJ).

147 MP) signaling at the neuromuscular junction (NMJ).

148 he Drosophila larval neuromuscular junction (NMJ).

149 ptor labeling at the neuromuscular junction (NMJ).

150 rve terminals of the neuromuscular junction (NMJ).

151 tic structure of the neuromuscular junction (NMJ).

152 enesis at the larval neuromuscular junction (NMJ).

153 show that at larval neuromuscular junctions (NMJ), motor neuron expression of wild-type human PFN1 in

154 Neuromuscular junctions (NMJs) are critical for survival and daily functioning.

155 zones in mammalian neuromuscular junctions (NMJs) at sub-diffraction limited resolution remains unkn

156 mammals age, their neuromuscular junctions (NMJs) gradually change their form, acquiring an increasi

157 and maintenance of neuromuscular junctions (NMJs) remains largely unknown.

158 studying Drosophila neuromuscular junctions (NMJs) we show that AZs consist of nano-modular release s

159 At larval neuromuscular junctions (NMJs), DCAF12 is expressed presynaptically in synaptic b

160 d their output, the neuromuscular junctions (NMJs), has been considered a key factor in the detriment

161 At mammalian neuromuscular junctions (NMJs), prolonged inactivity leads to muscle denervation

162 previously damaged neuromuscular junctions (NMJs), suggesting that the beneficial effects of iMuSCs

163 mbryonic Drosophila neuromuscular junctions (NMJs), where low-frequency Ca(2+) oscillations are requi

164 rom degeneration of neuromuscular junctions (NMJs), which form the connection between MNs and muscle

165 eptive synapses and neuromuscular junctions (NMJs), while having no effects on motor neuron death.

166 ound defects of the neuromuscular junctions (NMJs).

167 Syt4 at Drosophila neuromuscular junctions (NMJs).

168 synapses at larval neuromuscular junctions (NMJs).

169 ured with MNs, were able to form even larger NMJs.

170 l synaptic function and plasticity at larval NMJs.

171 ly independent functions of DCAF12 at larval NMJs.

172 ipts involved in establishing or maintaining NMJ structure.

173 t during the dry season, toad (Bufo marinus) NMJs display decreased sensitivity to extracellular calc

174 arget of the SMN protein and that mitigating NMJ defects may be one strategy in treating human spinal

175 intact, likely operate suboptimally at most NMJs of CMT2D mice.

176 ecular architecture of active zones in mouse NMJs at sub-diffraction limited resolution, and describe

177 localization of these two proteins in mouse NMJs revealed using dual-color stimulated emission deple

178 ed in the postsynaptic compartment of mutant NMJs include reduced glutamate receptor field size, and

179 duction of release at a proportion of mutant NMJs.

180 Smaller mutant NMJs with correspondingly fewer vesicles and partial den

181 (AChR), although there are aspects of normal NMJ development and function that need to be better unde

182 The absence of NMJ pathology is in stark contrast to what is found in r

183 s study was to examine how the alteration of NMJ physiology contributes to Pompe disease pathology; w

184 physiological, and histochemical analyses of NMJ-related measures of the tibialis anterior muscles of

185 acrophage-derived Vegf is a key component of NMJ recovery after injury.

186 We analyzed expression of NMJ-related genes, in situ muscle force production, and

187 asticity, a fundamental and adaptive form of NMJ plasticity in which perturbation to postsynaptic neu

188 s is known about the molecular mechanisms of NMJ aging although its structure and function are impair

189 Nevertheless, underlying mechanisms of NMJ formation was not well understood.

190 ouse models to investigate the mechanisms of NMJ reinnervation in both sexes, specifically whether ma

191 rom a set of ten new validated regulators of NMJ growth, we discovered that miR-34 mutants display sy

192 Quantal analysis of NMJs in two different mouse models of CMT2D (Gars(P278KY

193 ic transmission and morphological changes of NMJs have been explored in two nerve-muscle preparations

194 ing age- and disease-related degeneration of NMJs.

195 tion to maintain the structural integrity of NMJs.

196 and maintaining the structural integrity of NMJs.

197 tability in the formation and maintenance of NMJs remain poorly described.

198 ssociation with the postsynaptic membrane of NMJs.

199 s this gap in information, the morphology of NMJs was examined in two mouse models of SBMA, a myogeni

200 The observed pathology of NMJs in diseased SBMA mice is likely the morphological c

201 sential role of iMuSCs in the restoration of NMJs related to injuries and diseases.

202 ed with controls: (1) the number and size of NMJs was markedly increased in Syb2 (-/-) and Syb1(lew/l

203 tes to the organization and the stability of NMJs.

204 cular junction (NMJ), end-plate structure of NMJs and muscle contractility of semitendinosus muscles.

205 tion and removal to control the structure of NMJs.

206 The ultrastructure of NMJs revealed additional pathology, including deficits i

207 C in muscles or motoneurons had no effect on NMJ formation in either sex of mice, but the muscle muta

208 rated a more prolonged detrimental effect on NMJ reinnervation and worse functional muscle recovery.

209 e output of motor neurons, but its impact on NMJ repair remains unknown.

210 rker of glial axonal debris phagocytosis, on NMJ denervation in SOD1 mice.

211 we examined the impact of deleting FGFBP1 on NMJs.

212 on morphological analyses were undertaken on NMJs of rectus abdominis obtained from patients undergoi

213 real-time, live imaging of axonal outgrowth, NMJ formation and muscle maturation, as well as synchron

214 -ALS mouse model, we identified postsynaptic NMJ defects in newborn homozygous mutants that were attr

215 evolve with disease progression but precede NMJ neurodegeneration.

216 (Rapsn), died soon after birth with profound NMJ deficits.

217 muscle-specific mutation led to progressive NMJ degeneration in vivo We showed that the mutation red

218 ss of function of these mutants in promoting NMJ remodeling.

219 ades of study, the inability to reconstitute NMJ glutamate receptor function using heterologous expre

220 effective in modifying parameters reflecting NMJ structure and function nor in force restoration desp

221 lysis revealed SC activity near regenerating NMJs.

222 ynapse, may impact their ability to regulate NMJ stability and repair.

223 vidence that PFN1 is important in regulating NMJ morphology and influences survival and locomotion in

224 s and are overactivated at disease-resistant NMJs [soleus muscle (SOL)] in SOD1(G37R) mice.

225 Ongoing research may reveal NMJ targets and pathways whose therapeutic modulation wi

226 At postnatal day 180 (P180), FF and S NMJs of SOD1 already showed, respectively, lower and hig

227 s of congenital myasthenia, including severe NMJs dismantlement, muscle weakness, and fatigability.

228 timulation, and (4) release failures at some NMJs with high-frequency, long-duration stimulation.

229 ice had fewer acetylcholine receptor-stained NMJs detected by fluorescent labelling, but following sa

230 nsmission was markedly reduced in Syb2 (-/-) NMJs and completely abolished in Syb1(lew/lew)Syb2 (-/-)

231 remains constant in Syb1(lew/lew)Syb2 (-/-) NMJs despite changing Ca(2+) levels.

232 a(2+)-insensitive in Syb1(lew/lew)Syb2 (-/-) NMJs, our findings suggest that synaptobrevin-based SNAR

233 pletely abolished in Syb1(lew/lew)Syb2 (-/-) NMJs.

234 markedly reduced in Syb1(lew/lew)Syb2 (-/-) NMJs; and (3) evoked neurotransmission was markedly redu

235 uscle fiber size, enhances the post-synaptic NMJ area, reduces the abnormal accumulation of intermedi

236 al NAMPT is important for pre-/post-synaptic NMJ function, and maintaining skeletal muscular function

237 We hypothesized that NMJ synaptic functions would be altered precociously in

238 We suggest that NMJ fragmentation per se is not a reliable indicator of

239 We conclude that NMJs remain structurally intact in rectus abdominis in b

240 The NMJ had significant levels of activated caspase-3 but li

241 whereas application of exogenous NMDA at the NMJ accelerates synapse elimination and increases muscle

242 c13 disrupting homeostatic plasticity at the NMJ also impair short-term memory when central neurons a

243 imply that a peripheral modification at the NMJ contributes to the maintenance of the learned respon

244 drugs which improve synaptic efficacy at the NMJ could be considered in treating the pathophysiology

245 These results show that glial cells at the NMJ elaborate an inappropriate response to NMJ degenerat

246 importance of cell-cell communication at the NMJ for the integrity and full functionality of this syn

247 or muscle, strengthens the connection at the NMJ in a Hebbian manner.

248 communication is ubiquitously altered at the NMJ in ALS.

249 a maladapted response to denervation at the NMJ in ALS.SIGNIFICANCE STATEMENT Understanding how the

250 e importance of cell-cell interaction at the NMJ in spinal muscular atrophy (SMA), X-linked spinal an

251 f action of beta2-adrenergic agonists at the NMJ is not fully understood.

252 However, a conundrum persists at the NMJ whereby persistent but incoherent opposite neurotran

253 At the NMJ, a homeostatic system detects impaired postsynaptic

254 Macrophage recruitment occurred at the NMJ, distant from the nerve injury site, to support func

255 tic Schwann cells (PSCs), glial cells at the NMJ, regulate morphological stability, integrity, and re

256 other proteins involved in processes at the NMJ, which would be consistent with the previous observa

257 c signaling contributes to plasticity at the NMJ.

258 lutamate receptors are also expressed at the NMJ.

259 BMP receptor-containing compartments at the NMJ.

260 observation that CK2 appears enriched at the NMJ.

261 se mutation on mRNA levels and evaluated the NMJ transmission in VAMP1(lew/lew) mice, observing neuro

262 reflect only modifications upstream from the NMJ, within the CNS.

263 In investigating how N88K impairs the NMJ, we uncovered a novel signaling pathway by which Agr

264 ear envelope, is critical to maintaining the NMJ in mice.

265 Here, we consider the biology of the NMJ and review emerging lines of investigation that are

266 transmission and structural integrity of the NMJ in a mouse model of DOK7-CMS.

267 ysiological techniques and microscopy of the NMJ were used to study the effect of salbutamol, a beta2

268 ng a protein involved in organization of the NMJ, and emphasize the importance of appropriate symptom

269 e, neuromuscular disorders, and aging of the NMJ, focusing on communications among motoneurons, muscl

270 ical stability, integrity, and repair of the NMJ, one could predict that PSC functions would be alter

271 account for the profound dysfunction of the NMJ.

272 grin-known to be a critical organizer of the NMJ.

273 manner, before structural alterations of the NMJ.

274 junction with histological assessment of the NMJ.

275 We also find that the NMJ is capable of inducing homeostatic signaling even wh

276 e of AChRs in the targeting of rapsyn to the NMJ in vivo SIGNIFICANCE STATEMENT: Rapsyn is required f

277 g that occurs upon the return of tSCs to the NMJ may have wider implications for the mechanisms gover

278 in Schwann cells already associated with the NMJ, indicating that it is a marker of differentiated PS

279 e impairment of synaptic transmission at the NMJs.

280 Here, we examine the NMJs in mutant mouse embryos lacking either synaptobrevi

281 naptic vesicle endocytosis/exocytosis in the NMJs.

282 sent findings show that the structure of the NMJs suffered limited level of remodeling, suggesting a

283 ce lacking the FE65/FE65L1 binding site, the NMJs of APLP2/FE65-DKO and APLP2/FE65L1-DKO mice were an

284 The 'NMJ chip' enables real-time, live imaging of axonal outg

285 As their NMJ deficits resemble those of mutant APP/APLP2-DKO mice

286 (TGF-beta1) in skeletal muscles and at their NMJs.

287 arvae persist for 35 days, during which time NMJs exhibit extensive overgrowth in muscle size, presyn

288 dysfunction or deficiency may contribute to NMJ deficits in aged muscles.

289 dysfunction or deficiency may contribute to NMJ deficits in aged muscles.SIGNIFICANCE STATEMENT This

290 Multiple mechanisms contribute to NMJ repair and maintenance; however muscle stem cells (s

291 red even before denervation, contributing to NMJ malfunctions.

292 of SCs at P30, after NMJ maturation, led to NMJ fragmentation and neuromuscular transmission deficit

293 The mechanisms related to NMJ reinnervation are not known.

294 e NMJ elaborate an inappropriate response to NMJ degeneration in a manner that reflects motor-unit (M

295 the pre-and postsynaptic morphology of toads NMJs from the dry (inactive) and wet (active) seasons.

296 transiently increased at disease-vulnerable NMJs (STM muscle).

297 ether this is the case at disease-vulnerable NMJs and whether it translates into an impairment of PSC

298 eveal that glial cells at disease-vulnerable NMJs often fail to guide compensatory nerve terminal spr

299 nerve terminal sprouts at disease-vulnerable NMJs, a phenomenon essential for compensatory reinnervat

300 y affected by neuromuscular disease, whether NMJs in SBMA are similarly affected by disease is not kn

301 een identified ten proteins co-evolving with NMJ glutamate receptors.